EXPOsOMICS is a European Union funded project that aims to develop a novel approach to the assessment of exposure to high priority environmental pollutants, by characterizing the external and the ...internal components of the exposome. It focuses on air and water contaminants during critical periods of life. To this end, the project centres on 1) exposure assessment at the personal and population levels within existing European short and long-term population studies, exploiting available tools and methods which have been developed for personal exposure monitoring (PEM); and 2) multiple “omic” technologies for the analysis of biological samples (internal markers of external exposures). The search for the relationships between external exposures and global profiles of molecular features in the same individuals constitutes a novel advancement towards the development of “next generation exposure assessment” for environmental chemicals and their mixtures. The linkage with disease risks opens the way to what are defined here as ‘exposome-wide association studies’ (EWAS).
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
Recent studies have proven that tobacco smoke is a multipotent carcinogenic mixture that can cause cancer in many different organs. In addition, exposure to secondhand tobacco smoke is also ...carcinogenic to the human lung.
Summary Background Associations between circulating concentrations of oestrogens, progesterone, and androgens with breast cancer and related risk factors in premenopausal women are not well ...understood. We aimed to characterise these associations with a pooled analysis of data from seven studies. Methods Individual participant data for prediagnostic sex hormone and sex hormone-binding globulin (SHBG) concentrations were contributed from seven prospective studies. We restricted analyses to women who were premenopausal and younger than 50 years at blood collection, and to women with breast cancer diagnosed before age 50 years. We estimated odds ratios (ORs) with 95% CIs for breast cancer associated with hormone concentrations by conditional logistic regression in cases and controls matched for age, date of blood collection, and day of cycle, with stratification by study and further adjustment for cycle phase. We examined associations of hormones with risk factors for breast cancer in control women by comparing geometric mean hormone concentrations in categories of these risk factors, adjusted for study, age, phase of menstrual cycle, and body-mass index (BMI). All statistical tests were two-sided. Findings We included data for up to 767 women with breast cancer and 1699 controls in the risk analyses. Breast cancer risk was associated with a doubling in concentrations of oestradiol (OR 1·19, 95% CI 1·06–1·35), calculated free oestradiol (1·17, 1·03–1·33), oestrone (1·27, 1·05–1·54), androstenedione (1·30, 1·10–1·55), dehydroepiandrosterone sulphate (1·17, 1·04–1·32), testosterone (1·18, 1·03–1·35), and calculated free testosterone (1·08, 0·97–1·21). Breast cancer risk was not associated with luteal phase progesterone (doubling in concentration OR 1·00, 95% CI 0·92–1·09), and adjustment for other factors had little effect on any of these ORs. Cross-sectional analyses in control women showed several associations of sex hormones with breast cancer risk factors. Interpretation Circulating oestrogens and androgens are positively associated with the risk for breast cancer in premenopausal women. Funding Cancer Research UK.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Drinking water in much of Asia, particularly in coastal and rural settings, is provided by a variety of sources, which are widely distributed and frequently managed at an individual or local ...community level. Coastal and near-inland drinking water sources in South and South East (SSE) Asia are vulnerable to contamination by seawater, most dramatically from tropical cyclone induced storm surges. This paper assesses spatial vulnerabilities to salinisation of drinking water sources due to meteorological variability and climate change along the (ca. 6000 km) coastline of SSE Asia. The risks of increasing climatic stresses are first considered, and then maps of relative vulnerability along the entire coastline are developed, using data from global scale land surface models, along with an overall vulnerability index. The results show that surface and near-surface drinking water in the coastal areas of the mega-deltas in Vietnam and Bangladesh-India are most vulnerable, putting more than 25 million people at risk of drinking ‘saline’ water. Climate change is likely to exacerbate this problem, with adverse consequences for health, such as prevalence of hypertension and cardiovascular diseases. There is a need for identifying locations that are most at risk of salinisation in order for policy makers and local officials to implement strategies for reducing these health impacts. To counter the risks associated with these vulnerabilities, possible adaptation measures are also outlined. We conclude that detailed and fine scale vulnerability assessments may become crucial for planning targeted adaptation programmes along these coasts.
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CEKLJ, EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
A carbohydrate‐rich diet, resulting in high blood glucose and insulin, has been hypothesized as involved in colorectal cancer etiology. We investigated dietary glycemic index (GI) and glycemic load ...(GL), in relation to colorectal cancer, in the prospectively recruited EPIC‐Italy cohort. After a median 11.7 years, 421 colorectal cancers were diagnosed among 47,749 recruited adults. GI and GL were estimated from validated food frequency questionnaires. Multivariable Cox modeling estimated hazard ratios (HRs) for associations between colorectal cancer and intakes of total, high GI and low GI carbohydrate and GI and GL. The adjusted HR of colorectal cancer for highest versus lowest GI quartile was 1.35; 95% confidence interval (CI) 1.03–1.78; p trend 0.031. Increasing high GI carbohydrate intake was also significantly associated with increasing colorectal cancer risk (HR 1.45; 95% CI 1.04–2.03; p trend 0.034), whereas increasing low GI carbohydrate was associated with reducing risk (HR 0.73; 95% CI 0.54–0.98; p trend 0.033). High dietary GI and high GI carbohydrate were associated with increased risks of cancer at all colon sites (HR 1.37; 95% CI 1.00–1.88, HR 1.80; 95% CI 1.22–2.65, respectively), whereas high GI carbohydrate and high GL were associated with increased risk of proximal colon cancer (HR 1.94; 95% CI 1.18–3.16, HR 2.01; 95% CI 1.08–3.74, respectively). After stratification for waist‐to‐hip ratio (WHR), cancer was significantly associated with GI, and high GI carbohydrate, in those with high WHR. These findings suggest that high dietary GI and high carbohydrate intake from high GI foods are associated with increased risk of colorectal cancer.
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Diets rich in carbohydrate trigger increases in blood glucose and insulin levels, events that may be involved in the etiology of colorectal cancer. But carbohydrates vary in their impact on blood glucose levels, reflected in their glycemic index (GI) values, and whether high GI carbohydrates raise cancer risk remains much debated. Here, high dietary GI and elevated intake of carbohydrates from high GI foods were associated with increased risk of colorectal cancer. A diet rich in low GI carbohydrates, by contrast, was associated with a reduced risk of disease.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Abstract Objectives To investigate the association between environmental tobacco smoke, plasma cotinine concentration, and respiratory cancer or death. Design Nested case-control study within the ...European prospective investigation into cancer and nutrition (EPIC). Participants 303 020 people from the EPIC cohort (total 500 000) who had never smoked or who had stopped smoking for at least 10 years, 123 479 of whom provided information on exposure to environmental tobacco smoke. Cases were people who developed respiratory cancers or died from respiratory conditions. Controls were matched for sex, age (plus or minus 5 years), smoking status, country of recruitment, and time elapsed since recruitment. Main outcome measures Newly diagnosed cancer of lung, pharynx, and larynx; deaths from chronic obstructive pulmonary disease or emphysema. Plasma cotinine concentration was measured in 1574 people. Results Over seven years of follow up, 97 people had newly diagnosed lung cancer, 20 had upper respiratory cancers (pharynx, larynx), and 14 died from chronic obstructive pulmonary disease or emphysema. In the whole cohort exposure to environmental tobacco smoke was associated with increased risks (hazard ratio 1.30, 95% confidence interval 0.87 to 1.95, for all respiratory diseases; 1.34, 0.85 to 2.13, for lung cancer alone). Higher results were found in the nested case-control study (odds ratio 1.70, 1.02 to 2.82, for respiratory diseases; 1.76, 0.96 to 3.23, for lung cancer alone). Odds ratios were consistently higher in former smokers than in those who had never smoked; the association was limited to exposure related to work. Cotinine concentration was clearly associated with self reported exposure (3.30, 2.07 to 5.23, for detectable/non-detectable cotinine), but it was not associated with the risk of respiratory diseases or lung cancer. Frequent exposure to environmental tobacco smoke during childhood was associated with lung cancer in adulthood (hazard ratio 3.63, 1.19 to 11.11, for daily exposure for many hours). Conclusions This large prospective study, in which the smoking status was supported by cotinine measurements, confirms that environmental tobacco smoke is a risk factor for lung cancer and other respiratory diseases, particularly in ex-smokers.
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BFBNIB, CMK, NMLJ, NUK, PNG, SAZU, UL, UM, UPUK
In this paper I wish to introduce some ideas about scientific reasoning that have reached the epidemiological community only marginally. They have to do with how we classify things (diseases), and ...how we formulate hypotheses (causes). According to a simplified and currently untenable model, we come to defining what a disease, or a protone or a chromosome, is by progressive simplification—that is, by extracting an essence from the individual characters of disease. At the end of this inductive process a single element, which guarantees the unequivocal inclusion in the category, is identified. This is what has been called “Merkmal-definition” (Merkmal meaning distinctive sign)—that is, the definition of disease would be allowed by the isolation of a crucial property, a necessary and sufficient condition, which makes that disease unique (and a chair out of a chair, a proton out of a proton, etc). However many objections have been raised by Wittgenstein, Eleanor Rosch and others to this idea: a Merkmal is not always identifiable, and more often a word is used to indicate not a homogeneous and unequivocal set of observations, but a confused constellation with blurred borders. This constellation has been called a fuzzy set and is at the basis of the semantic theory of metaphors proposed by MacCormac and the prototype theory proposed by Rosch. In this way the concept of disease, for example, abandons monothetic definitions, amenable to a necessary and sufficient characteristic, to become “polythetic.” I explain how these concepts can help medicine and epidemiology to clarify some open issues in the definition of disease and the identification of causes, through examples taken from oncology, psychiatry, cardiology and infectious diseases. The definition of a malignant tumour, for example, seems to correspond to the concept of “family resemblance,” since there is no single criterion that allows us to define unequivocally the concept of cancer: not morphology (there are borderline situations between benign and malignant), not clinical features, not biochemical or molecular lesions. In the case of schizophrenia, the problem of indetermination, as it has been defined, is even stronger. Mental disease probably cannot be distinguished from health in a clearcut way (according to a minimum set of necessary criteria), but it would have a fuzzy border with mental conditions that characterise normal subjects, through intermediate linking conditions.
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BFBNIB, CMK, NMLJ, NUK, PNG, SAZU, UL, UM, UPUK
In overviews concerning environmental cancers, the definition of ‘environmental’ can vary considerably in terms of the list of exposures considered, due to differences in inclusion criteria, and the ...articles tend to focus mainly or exclusively on Western populations. International agencies such as World Health Organisation, that have had considerable success in fighting infectious diseases, seem to be weaker when considering the relevance of environmental carcinogens, particularly in developing countries, and in identifying the exposed populations. The purpose of this paper is to reexamine the issue with a specific focus on developing countries. There are good reasons to believe that the burden of environmental cancers in such countries is high and has been underestimated in previous analyses. We examine the most common pollutants (aflatoxins, arsenic, air pollutants, biomass fuel and coal, polychlorinated biphenyls and wastes). A systematic review was not possible given the sparse nature of the data, but we suggest that the burden of environmental exposures to carcinogens can be substantial in developing countries.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
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